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Inhibitory effect of vitexicarpin TNF‐α‐induced vascular inflammation in human umbilical vein endothelial cells
Author(s) -
Lee So Min,
Lee Yun Jung,
Kim Jin Sook,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.784.7
Subject(s) - umbilical vein , inflammation , tumor necrosis factor alpha , cell adhesion molecule , e selectin , cell adhesion , human umbilical vein endothelial cell , intercellular adhesion molecule 1 , endothelial stem cell , chemistry , soluble cell adhesion molecules , intercellular adhesion molecule , icam 1 , microbiology and biotechnology , immunology , biology , cell , biochemistry , in vitro
Vascular inflammation is pivotal event in the pathogenesis of many human diseases, including atherosclerosis. Recent pharmacological studies have demonstrated that vitexicarpin, flavonoid isolated from Vitex rotundifolia , was found to show potent inhibition against lymphocyte proliferation and inflammation. In this study, we investigated whether vitexicarpin prevented tumor necrosis factor‐alpha (TNF‐α)‐induced vascular inflammation in primary cultured human umbilical vein endothelial cells (HUVEC). We found that pretreatment with vitexicarpin decreased TNF‐α (10 ng/ml)‐induced of cell adhesion molecules (CAMs) such as vascular cell adhesion molecule‐1 (VCAM‐1), intracellular adhesion molecule‐1 (ICAM‐1) and endothelial cell selectin (E‐selectin) as well as matrix metalloproteinase‐2, ‐9 (MMP‐2/‐9) expression in HUVEC. Vitexicarpin significantly inhibited the TNF‐α‐induced increase in HL‐60 monocyte adhesion to HUVEC. Vitexicarpin significantly decreased TNF‐α‐induced intracellular ROS production. Furthermore, vitexicarpin inhibited TNF‐α‐induced transcriptional activity of NF‐κB p65 and IκB‐α phosphorylation. In conclusion, vitexicarpin significantly reduced the increased vascular inflammation, through out inhibition of ROS‐NF‐κB pathway in HUVEC.